Hyperaldosteronim

Question 1

Low BP is sensed in glomerulus trigger of _____ from JG cells

Answer 1

renin

Question 2

catalyzes of cleavage of Ang I from angiotensinogen the to ang II via

Answer 2

ACE

Question 3

How does Ang II increase BP

Answer 3

causes vasoconstriction and increaes aldosterone release from the zona glomerulosa of adrenal cortex

Question 4

Aldosterone works in dista tubule to affect Na and K balance.. Aldosterone will ______ Na+ thus get retnetion of Na in body. In response, K and Hyrogen will be _____ in the tuble

leads to overall:

Answer 4

Na resorbed

thus K and H will get secreated

end up with fluid retention and increased blood volume

Question 5

drug to inhibit renin that works to decrease renin activity, but will see increased renin protein consentrtaions

Answer 5

Aliskiren

Question 6

Adrenal glands (from adenoma or one adrenal or both adrenals w/ hyperplasia) secreate excessive aldosterone that is AUTONOMOUS and not being controlled by:

Answer 6

renin and ang II

should see negative feedback as aldosterone increases

Question 7

What is a result of excessive aldosterone

Answer 7

increased urinary potassium loss and hypertension (d/t excessive Na+ and fluid retention) with clinical presentation of Hypertension and Hypokalemia

Question 8

Hypertension and Hyperkalemia are often seen in

Answer 8

hyperaldosteronism

Question 9

pt comes in with Low K and high BP… what should we do?

Answer 9

consider test for primary hyperaldosteronism

also: resistant HTN, adrenal incidentaloma and HTN; onset of THN at young age <30 yr

Question 10

We are thinking our patient has secondary hypertension, what kind of testing should we look into?

Answer 10

Morning blood sample in seated ambulant patient:

-Plasma aldosterone concentration (PAC)

Plasma renin activity (PRA) or plasma renin concentration

Question 11

To make Dx of primary hyperaldosteronism, measure an incresaed ratio of:

Answer 11

Plasma Aldosterone : Plasma Renin (with potassium replete)

Question 12

Aldosterone increasesd in pirmary hyperaldosteronism due to:

Answer 12

autonomous secreation from adrenal adenoma

Question 13

Why is renin suppressed in pirmary hyperaldosteronism?

Answer 13

suppressed dt increaed blood pressure (baro reflex) and increased sodium (from increased reabsorption)

Question 14

Pt has HTN and HYPOkalemia

see pt with resistant HTN

early onset HTN or very severe HTN

all signs of

Answer 14

Primary aldosteronism

Question 15

What levels would we see to confirm primary aldosteronism:

PAC (plasma aldosterone concentration) and

PRA (plasma renin activity)

Answer 15

see HIGH aldosterone and LOW renin

or

Aldosterone:Renin ratio > 20

Question 16

Aldosterone secreating adrenocortical adenoma adn bilateral hyperplasia of Zona Glomerulosa can cause:

Answer 16

Primary Hyperaldosteronism

Question 17

Renal ischemia, decreased intravascular volume, CHF, chrnoic diuretics, hypoproteinemic states, Na-wasting disorders and chronic renal fail can all cause:

Answer 17

Secondary Hyperaldosteronism

Question 18

Renin ischeia increases renin secreation from:

Answer 18

JG cells

Question 19

CHF increases renin secration via:

Answer 19

baroreflex

Question 20

Diuretic/laxatives increase renin because of

Answer 20

sodium and volume loss

Question 21

ONce a dx of primary adlosteronism has been made you need to determine if this is from unilateral or bilateral adrenal source… what do we order?

Answer 21

CT scan of adrenal glands or AVS or sampling of what the adrenal glands are draining

Question 23

The result of excess aldosterone produciton in response to increased RAAS activity

Answer 23

secondary hyperaldosteornism

Question 24

What do we use to distinguish difference between primary and secondary hyperaldosteronism

Answer 24

Renin levels increase in secondary forms where as in primary renin decresaes

Question 25

What needs to happen before we do a scan to determine cause of hyperaldosteronism?

Answer 25

need to have a biochemical confirmaiton

Question 26

You get a CT or MRI of pt with hyperaldosteronism and it shows they ahve a unilateral adrenal tumor… what is the treamtement?

Question 27

You get a CT or MRI of pt with hyperaldosteronism and it shows they ahve a bilateral adrenal abnormality… what is the next step?

Answer 27

Perform a selective venous catherteriszation for aldosterone and cortisol to see if you can identify source: if unilateral do adrenalectomy

if bilateral, you can’t take out both adrenals, thus do medicla management

Question 28

What medicaitons are used to mange pts with bilateral hyperaldosteronism?

Answer 28

need to block aldosterone at the level of the receptor:

spironolactone or eplereonone

Question 29

MOA of spilarinone or eplereinone

Answer 29

Competitive receptor antagonists of aldosterone

result in decreasing Na dn water retention and increase serum potassium

Question 30

Glycyrrhizic acid can decrease activity of what enZ?

Answer 30

11-HSD2 ; see hypertention and hypokalemia

Question 31

caused by 11HSD2 impairment thus dont convert cortisol to cortisone and increase cortisol action on the mineralcorticoid receptor in the kidney (mimics aldosterone)

Answer 31

Apparent mineralcorticoid excess

Question 32

AME causes what symptoms?

Answer 32

Hypertention and hypokalemia, metabolic alkasosis, low renin acitivty, normal plamsa cortisal levels

Question 33

Pt is prsenting like they ahve primary hyperaldosteronism but lack high aldosteorne levels

Answer 33

Liddle syndrome

Question 34

Cuase of Liddle syndrome

Answer 34

mutation in amiloride-sensitizing epithelial Na channel thus see increased activity of Na channel and increase Na reabsorption, K+ wasting, HTN and Hypokalemia

Question 35

What do pts with Liddle sydrome have as far as renin and aldosterone levels?

Answer 35

Liddle

Low renin

Low aldosterone

Question 36

What is our most importatn protector from hyperkalemia

Answer 36

aldosterone

as K increases, so does aldosterone to get rid of it